Athreya Rangavajhula
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Athreya Rangavajhula has a total of 42 co-authors. Here are the top co-authors by number of shared publications:
- Amy C. Fan
University of California San Francisco 4 Department of Pathology San Francisco, CA
21 shared publications - Daiki Karigane
Department of Stem Cell Biology, Research Institute, National Center for Global Health and Medicine
21 shared publications - Fabian P. Suchy
Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA, USA
21 shared publications - Hiromitsu Nakauchi
Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, USA
21 shared publications - Jonas L. Fowler
Stanford University 3 Department of Developmental Biology and Institute for Stem Cell Biology and Regenerative Medicine Stanford, California
21 shared publications - Kensuke Kayamori
Division of Stem Cell and Molecular Medicine, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan
21 shared publications
Latest Publications
- Open Access
Non-cell-autonomous removal of protein aggregates via trogocytosis
Protein aggregate formation can cause cell damage and contribute to tissue pathologies including neurodegeneration. Protein aggregates are normally eliminated by cell-intrinsic mechanisms of lysosomal (autophagic) degradation. However, degradative capacity varies between cell types, raising the possibility that high-capacity cell types, such as macrophages, may contribute to aggregate disposal from the low-capacity cells. Here, we show that cellular protein aggregates are removed by macrophages via trogocytosis — a partial engulfment of the target cells. Lysosomal stress upon protein aggregate accumulation promotes cell surface expression of the transmembrane isoform of the macrophage growth factor CSF1 (tmCSF1), which is detected by macrophages through the CSF1 receptor to drive trogocytosis. Insufficient or impaired degradation of protein aggregates in lysosomes results in their transport along microtubules to the plasma membrane where they physically associate with tmCSF1. This enables macrophages to specifically trogocytose protein aggregates. These findings reveal a protein homeostasis system that eliminates protein aggregates in a non-cell-autonomous manner.
Open AccessNon-cell-autonomous removal of protein aggregates via trogocytosis
Protein aggregate formation can cause cell damage and contribute to tissue pathologies including neurodegeneration. Protein aggregates are normally eliminated by cell-intrinsic mechanisms of lysosomal (autophagic) degradation. However, degradative capacity varies between cell types, raising the possibility that high-capacity cell types, such as macrophages, may contribute to aggregate disposal from the low-capacity cells. Here, we show that cellular protein aggregates are removed by macrophages via trogocytosis — a partial engulfment of the target cells. Lysosomal stress upon protein aggregate accumulation promotes cell surface expression of the transmembrane isoform of the macrophage growth factor CSF1 (tmCSF1), which is detected by macrophages through the CSF1 receptor to drive trogocytosis. Insufficient or impaired degradation of protein aggregates in lysosomes results in their transport along microtubules to the plasma membrane where they physically associate with tmCSF1. This enables macrophages to specifically trogocytose protein aggregates. These findings reveal a protein homeostasis system that eliminates protein aggregates in a non-cell-autonomous manner.
- Open Access
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Data S5 from DNMT3A R882H Is Not Required for Disease Maintenance in Primary Human AML but Is Associated with Increased Leukemia Stem Cell Frequency
Plots of top 100 DMRs (by area statistic & FWER) between DNMT3AR882H/WT re-mutated and DNMT3AWT/WT samples for AML-derived iPSC iSU444 at 8 months
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Data S5 from DNMT3A R882H Is Not Required for Disease Maintenance in Primary Human AML but Is Associated with Increased Leukemia Stem Cell Frequency
Plots of top 100 DMRs (by area statistic & FWER) between DNMT3AR882H/WT re-mutated and DNMT3AWT/WT samples for AML-derived iPSC iSU444 at 8 months
- Open Access
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table S4 from DNMT3A R882H Is Not Required for Disease Maintenance in Primary Human AML but Is Associated with Increased Leukemia Stem Cell Frequency
DMRs between DNMT3AR882H re-mutated and DNMT3AWT corrected blasts for patients SU372C, SU540, and SU575; and for AML-derived iPSC iSU444
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S4 from DNMT3A R882H Is Not Required for Disease Maintenance in Primary Human AML but Is Associated with Increased Leukemia Stem Cell Frequency
DMRs between DNMT3AR882H re-mutated and DNMT3AWT corrected blasts for patients SU372C, SU540, and SU575; and for AML-derived iPSC iSU444
- Open Access
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table S8 from DNMT3A R882H Is Not Required for Disease Maintenance in Primary Human AML but Is Associated with Increased Leukemia Stem Cell Frequency
Enrichment of upstream regulators in DMR-associated genes and differentially expressed genes from Ingenuity Pathway Analysis
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S8 from DNMT3A R882H Is Not Required for Disease Maintenance in Primary Human AML but Is Associated with Increased Leukemia Stem Cell Frequency
Enrichment of upstream regulators in DMR-associated genes and differentially expressed genes from Ingenuity Pathway Analysis
- Open Access
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Data S6 from DNMT3A R882H Is Not Required for Disease Maintenance in Primary Human AML but Is Associated with Increased Leukemia Stem Cell Frequency
Plots of top 100 DMRs (by area statistic & FWER) between DNMT3AR882H/WT re-mutated and DNMT3AWT/WT samples for patient SU372C at 8 months
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Data S6 from DNMT3A R882H Is Not Required for Disease Maintenance in Primary Human AML but Is Associated with Increased Leukemia Stem Cell Frequency
Plots of top 100 DMRs (by area statistic & FWER) between DNMT3AR882H/WT re-mutated and DNMT3AWT/WT samples for patient SU372C at 8 months
- Open Access
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table S3 from DNMT3A R882H Is Not Required for Disease Maintenance in Primary Human AML but Is Associated with Increased Leukemia Stem Cell Frequency
Summary of DMRs between DNMT3AR882H re-mutated and DNMT3AWT corrected blasts for patients SU372C, SU540, and SU575; and for AML-derived iPSC iSU444
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S3 from DNMT3A R882H Is Not Required for Disease Maintenance in Primary Human AML but Is Associated with Increased Leukemia Stem Cell Frequency
Summary of DMRs between DNMT3AR882H re-mutated and DNMT3AWT corrected blasts for patients SU372C, SU540, and SU575; and for AML-derived iPSC iSU444
- Open Access
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table S2 from DNMT3A R882H Is Not Required for Disease Maintenance in Primary Human AML but Is Associated with Increased Leukemia Stem Cell Frequency
FACS staining panels used in this study
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S2 from DNMT3A R882H Is Not Required for Disease Maintenance in Primary Human AML but Is Associated with Increased Leukemia Stem Cell Frequency
FACS staining panels used in this study
- Open Access
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table S5 from DNMT3A R882H Is Not Required for Disease Maintenance in Primary Human AML but Is Associated with Increased Leukemia Stem Cell Frequency
Genes mapping to DMRs significant between DNMT3AR882H re-mutated and DNMT3AWT corrected blasts in all three patients (SU372C, SU540, and SU575)
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S5 from DNMT3A R882H Is Not Required for Disease Maintenance in Primary Human AML but Is Associated with Increased Leukemia Stem Cell Frequency
Genes mapping to DMRs significant between DNMT3AR882H re-mutated and DNMT3AWT corrected blasts in all three patients (SU372C, SU540, and SU575)
- Open Access
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Data S1 from DNMT3A R882H Is Not Required for Disease Maintenance in Primary Human AML but Is Associated with Increased Leukemia Stem Cell Frequency
Plots of top 100 DMRs (by area statistic & FWER) between DNMT3AR882H/WT re-mutated and DNMT3AWT/WT samples for patient SU372C at 4 months
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Data S1 from DNMT3A R882H Is Not Required for Disease Maintenance in Primary Human AML but Is Associated with Increased Leukemia Stem Cell Frequency
Plots of top 100 DMRs (by area statistic & FWER) between DNMT3AR882H/WT re-mutated and DNMT3AWT/WT samples for patient SU372C at 4 months
- Open Access
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table S6 from DNMT3A R882H Is Not Required for Disease Maintenance in Primary Human AML but Is Associated with Increased Leukemia Stem Cell Frequency
Overlap between DMRs (DNMT3AR882H/WT versus DNMT3AWT/WT) and DNA methylation canyons, stratified by patient and canyon type
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S6 from DNMT3A R882H Is Not Required for Disease Maintenance in Primary Human AML but Is Associated with Increased Leukemia Stem Cell Frequency
Overlap between DMRs (DNMT3AR882H/WT versus DNMT3AWT/WT) and DNA methylation canyons, stratified by patient and canyon type